HEMAGGLUTINATION 49 



A few Strains show a more limited ability. If strain i were one of 

 these it might be found that it can destroy all strain i inhibitor in 

 preparation A but cannot destroy completely the inhibitors for strains 

 2, 3, 4 etc. With preparation B however, strain i might be able to 

 destroy the entire complex. This suggests that a restricted degree of 

 enzyme specificity exists and also that there are qualitative differences 

 in what is measured as strain i inhibitor between preparation of differ- 

 ent sources. 



In attempting to explain this evidence we may assume that there 

 exists a spectrum of inhibitors or receptors, each with somewhat differ- 

 ent affinities for various strains of this group and vdth different suscep- 

 tibilities to destruction by virus enzymes. Virus enzymes attack this 

 group of substrates in essentially similar fashion but with varying 

 degrees of efficiency or speed. In a few cases an enzyme cannot attack 

 parts of this substrate complex. 



This picture of virus-receptor relationships would be more inter- 

 esting if analogous systems could be found for other groups. There is 

 an isolated but clear cut example of this in strain 1233 (Hirst, 1950b), 

 an agent of respiratory infection in man, unrelated antigenically to the 

 MNI group but which elutes spontaneously from red cells and has a 

 receptor-inhibitor system quite unrelated to that which has been de- 

 scribed for mumps, influenza and Newcastle disease. 1233 can destroy 

 its own receptors in inhibitors but cannot attack those of the MNI 

 group and vice- versa. 



We must still face the somewhat speculative problem of what this 

 system means in respect to the steps occurring in natural infection. The 

 biological relationship of receptors and inhibitors is not clear though 

 they are similar in a number of respects. Inhibitors play no obvious 

 role in resistance to virus infection since they are readily liquidated 

 by the virus and even when present in high concentration have only 

 a weak effect on virus infectivity. Inhibitors may be chemically treated 

 (Fazekas de St. Groth, 1949) so that virus is unable to split them, in 

 which case the treated inhibitor becomes active in reducing the ability 

 of virus to infect, apparently in a manner similar to that of virus anti- 

 body. There is no evidence that inhibitors behave this way in nature. 



It has already been noted that virus receptors are produced by 

 many living cells, including those susceptible to virus infection, and 

 that intact receptors seem to be necessary for infection to take place. 

 What role does receptor destruction play in infection? Since receptors 

 occur on the surface of cells and since in red cell models the virus 

 destroys this substance, it was suggested that the reaction provided the 



